<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Corneveaux JJ</submitter><funding>NIA NIH HHS</funding><funding>Medical Research Council</funding><funding>Alzheimers Research UK</funding><funding>NINDS NIH HHS</funding><pagination>3295-301</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2908469</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>19(16)</volume><pubmed_abstract>In this study, we assess 34 of the most replicated genetic associations for Alzheimer's disease (AD) using data generated on Affymetrix SNP 6.0 arrays and imputed at over 5.7 million markers from a unique cohort of over 1600 neuropathologically defined AD cases and controls (1019 cases and 591 controls). Testing the top genes from the AlzGene meta-analysis, we confirm the well-known association with APOE single nucleotide polymorphisms (SNPs), the CLU, PICALM and CR1 SNPs recently implicated in unusually large data sets, and previously implicated CST3 and ACE SNPs. In the cases of CLU, PICALM and CR1, as well as in APOE, the odds ratios we find are slightly larger than those previously reported in clinical samples, consistent with what we believe to be more accurate classification of disease in the clinically characterized and neuropathologically confirmed AD cases and controls.</pubmed_abstract><journal>Human molecular genetics</journal><pubmed_title>Association of CR1, CLU and PICALM with Alzheimer's disease in a cohort of clinically characterized and neuropathologically verified individuals.</pubmed_title><pmcid>PMC2908469</pmcid><funding_grant_id>R01 AG034504</funding_grant_id><funding_grant_id>R01 AG015819</funding_grant_id><funding_grant_id>ART-PG2010-1</funding_grant_id><funding_grant_id>P30 AG019610</funding_grant_id><funding_grant_id>R01 NS059873</funding_grant_id><funding_grant_id>U01 AG016976</funding_grant_id><funding_grant_id>G0400074</funding_grant_id><funding_grant_id>K08 AG034290</funding_grant_id><funding_grant_id>G0701075</funding_grant_id><funding_grant_id>G0900652</funding_grant_id><funding_grant_id>G0502157</funding_grant_id><pubmed_authors>Meechoovet HB</pubmed_authors><pubmed_authors>Chewning K</pubmed_authors><pubmed_authors>Hardy J</pubmed_authors><pubmed_authors>Frost D</pubmed_authors><pubmed_authors>Gerber JD</pubmed_authors><pubmed_authors>Benson HL</pubmed_authors><pubmed_authors>Myers AJ</pubmed_authors><pubmed_authors>Craig DW</pubmed_authors><pubmed_authors>Chibnik LB</pubmed_authors><pubmed_authors>Engel A</pubmed_authors><pubmed_authors>Reiman EM</pubmed_authors><pubmed_authors>De Jager PL</pubmed_authors><pubmed_authors>Chen K</pubmed_authors><pubmed_authors>Singleton AB</pubmed_authors><pubmed_authors>Van Keuren-Jensen KR</pubmed_authors><pubmed_authors>Dunckley T</pubmed_authors><pubmed_authors>Shulman JM</pubmed_authors><pubmed_authors>Corneveaux JJ</pubmed_authors><pubmed_authors>Ramirez M</pubmed_authors><pubmed_authors>O'Reilly S</pubmed_authors><pubmed_authors>Bennett DA</pubmed_authors><pubmed_authors>Allen AN</pubmed_authors><pubmed_authors>Villa SE</pubmed_authors><pubmed_authors>Heward C</pubmed_authors><pubmed_authors>Lee W</pubmed_authors><pubmed_authors>Nalls MA</pubmed_authors><pubmed_authors>Pruzin JJ</pubmed_authors><pubmed_authors>Huentelman MJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Association of CR1, CLU and PICALM with Alzheimer's disease in a cohort of clinically characterized and neuropathologically verified individuals.</name><description>In this study, we assess 34 of the most replicated genetic associations for Alzheimer's disease (AD) using data generated on Affymetrix SNP 6.0 arrays and imputed at over 5.7 million markers from a unique cohort of over 1600 neuropathologically defined AD cases and controls (1019 cases and 591 controls). Testing the top genes from the AlzGene meta-analysis, we confirm the well-known association with APOE single nucleotide polymorphisms (SNPs), the CLU, PICALM and CR1 SNPs recently implicated in unusually large data sets, and previously implicated CST3 and ACE SNPs. In the cases of CLU, PICALM and CR1, as well as in APOE, the odds ratios we find are slightly larger than those previously reported in clinical samples, consistent with what we believe to be more accurate classification of disease in the clinically characterized and neuropathologically confirmed AD cases and controls.</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Aug</publication><modification>2020-11-19T08:56:21Z</modification><creation>2019-03-27T00:32:37Z</creation></dates><accession>S-EPMC2908469</accession><cross_references><pubmed>20534741</pubmed><doi>10.1093/hmg/ddq221</doi></cross_references></HashMap>